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The control of myocardial Ca++ sequestration with nifedipine cardioplegia
Insights
Nifedipine significantly reduces myocardial calcium sequestration during cardiopulmonary bypass (CPB) and reperfusion. This calcium control is linked to improved heart performance after surgery.
Area of Science:
- Cardiovascular Science
- Biochemistry
- Pharmacology
Background:
- Myocardial calcium sequestration is a critical factor during cardiac surgery.
- Cardiopulmonary bypass (CPB) and cardioplegic solutions can influence calcium balance.
- Understanding calcium regulation is key to improving myocardial protection.
Purpose of the Study:
- To investigate the effect of nifedipine on myocardial 45Ca sequestration during ischemia and reperfusion.
- To evaluate the efficacy of nifedipine combined with cardioplegia in controlling myocardial calcium.
- To correlate reduced calcium sequestration with improved myocardial performance post-CPB.
Main Methods:
- Studied myocardial 45Ca sequestration in dogs undergoing 60 minutes of global ischemia and 30 minutes of reperfusion using CPB.
- Administered a standard hyperkalemic cardioplegic solution (Group I) or the same solution plus nifedipine (Group II).
- Measured tissue and plasma specific activity (SA) of 45Ca, calculating relative specific activity (RSA) to assess sequestration.
Main Results:
- Nifedipine significantly decreased myocardial 45Ca sequestration compared to the standard cardioplegia group (p < 0.01).
- Group II showed substantially lower RSAs at 0, 20, and 30 minutes of reperfusion.
- While Group I RSA increased by 498% in the first 20 minutes of reperfusion, Group II RSA increased only by 23.8%.
Conclusions:
- Nifedipine effectively controls myocardial calcium sequestration during ischemia and reperfusion when used with hypothermic hyperkalemic cardioplegia.
- Reduced calcium sequestration is correlated with improved myocardial performance after CPB.
- Nifedipine offers a promising adjunct for myocardial protection during cardiac surgery.
Abstract:
Myocardial 45Ca sequestration was studied in dogs after an injection of 45CaCl2 during 60 minutes of global ischemia and 30 minutes of reperfusion using cardiopulmonary bypass (CPB) at 32 degrees C. Group I (n = 10) received a standard hyperkalemic cardioplegic solution and Group II (n = 10) received the same cardioplegia solution plus nifedipine (100 micrograms/300 cc). After aortic cross-clamping, 300 cc of cardioplegic solution was delivered at 0 and 30 minutes at 4 degrees C. Tissue specific activity (SA = cpm x 10(4)/gm) and plasma specific activity (SA = cpm x 10(4)/ml) were determined before release of the cross-clamp and serially by biopsy during reperfusion. The ratio of tissue SA to plasma SA, termed relative specific activity (RSA), indicates myocardial 45Ca sequestration. Nifedipine led to a marked decrease in sequestration. Group II RSAs were 31.5%, 82.1%, and 39.6% less than Group I RSAs at 0, 20, and 30 minutes of reperfusion. All differences were highly significant (p less than 0.01). During the first 20 minutes of reperfusion, the Group I RSA increased 498% while the Group II RSA increased only 23.8%. A correlation is shown between the decreased calcium sequestration and improved myocardial performance after CPB, demonstrated in previous experiments using nifedipine. Nifedipine in combination with a hypothermic hyperkalemic cardioplegic solution effectively controls myocardial calcium sequestration during 60 minutes of ischemia arrest and the immediate 30 minutes of reperfusion.